Lack of effects of 1439 MHz electromagnetic near field exposure on the blood-brain barrier in immature and young rats

2005 ◽  
Vol 26 (7) ◽  
pp. 578-588 ◽  
Author(s):  
Masanori Kuribayashi ◽  
Jianqing Wang ◽  
Osamu Fujiwara ◽  
Yuko Doi ◽  
Kyoko Nabae ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Near Field ◽  
Brain Barrier ◽  
Field Exposure ◽  
Young Rats ◽  
Blood Brain

Paroxysmal slow cortical activity in Alzheimer’s disease and epilepsy is associated with blood-brain barrier dysfunction

2019 ◽  
Vol 11 (521) ◽  
pp. eaaw8954 ◽  
Author(s):  
Dan Z. Milikovsky ◽  
Jonathan Ofer ◽  
Vladimir V. Senatorov ◽  
Aaron R. Friedman ◽  
Ofer Prager ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Causative Role ◽  
Barrier Dysfunction ◽  
Therapeutic Implications ◽  
Young Rats ◽  
Blood Brain ◽  
Nonconvulsive Seizures

A growing body of evidence shows that epileptic activity is frequent but often undiagnosed in patients with Alzheimer’s disease (AD) and has major therapeutic implications. Here, we analyzed electroencephalogram (EEG) data from patients with AD and found an EEG signature of transient slowing of the cortical network that we termed paroxysmal slow wave events (PSWEs). The occurrence per minute of the PSWEs was correlated with level of cognitive impairment. Interictal (between seizures) PSWEs were also found in patients with epilepsy, localized to cortical regions displaying blood-brain barrier (BBB) dysfunction, and in three rodent models with BBB pathology: aged mice, young 5x familial AD model, and status epilepticus–induced epilepsy in young rats. To investigate the potential causative role of BBB dysfunction in network modifications underlying PSWEs, we infused the serum protein albumin directly into the cerebral ventricles of naïve young rats. Infusion of albumin, but not artificial cerebrospinal fluid control, resulted in high incidence of PSWEs. Our results identify PSWEs as an EEG manifestation of nonconvulsive seizures in patients with AD and suggest BBB pathology as an underlying mechanism and as a promising therapeutic target.

Influence d'un retard de croissance sur la perméabilité de la barrière hémato-encéphalique chez le rat nouveau-né exposé au plomb

1984 ◽  
Vol 62 (1) ◽  
pp. 142-145 ◽  
Author(s):  
John Turnbull ◽  
Jules Brodeur
Keyword(s):  
Blood Brain Barrier ◽  
Growth Retardation ◽  
Trypan Blue ◽  
Normal Diet ◽  
Brain Barrier ◽  
Free Access ◽  
Postnatal Maturation ◽  
Young Rats ◽  
Nutritional Effect ◽  
Blood Brain

Postnatal administration of lead to young rats via maternal milk increases the permeability of the blood–brain barrier to trypan blue. However, since this regimen delays postnatal maturation, the question arises whether growth retardation per se could explain the altered permeability to the dye. The present investigation was undertaken to examine this possibility. A first group of newborn rats were fed by dams having free access to normal food; a second group was fed by dams receiving 3% lead as the acetate salt in their food; a third group was fed by dams whose normal diet was restricted to the amount taken daily by dams of the second group. Signs of encephalopathy as shown by urinary incompetence and hind-limb paralysis were observed only in young pups exposed to lead; similarly, only the latter showed increased brain permeability to trypan blue. These results suggest that the altered permeability of the blood–brain barrier in young rats is the direct consequence of lead toxicity and not of growth retardation secondary to a nutritional effect of lead.

Alterations in NADPH oxidase expression and blood–brain barrier in bile duct ligation-treated young rats: Effects of melatonin

2012 ◽  
Vol 60 (8) ◽  
pp. 751-758 ◽  
Author(s):  
Yu-Chieh Chen ◽  
Jiunn-Ming Sheen ◽  
You-Lin Tain ◽  
Chih-Cheng Chen ◽  
Miao-Meng Tiao ◽  
...  
Keyword(s):  
Bile Duct ◽  
Nadph Oxidase ◽  
Blood Brain Barrier ◽  
Bile Duct Ligation ◽  
Brain Barrier ◽  
Young Rats ◽  
Blood Brain ◽  
Duct Ligation
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